ライフサイエンスコーパス: soft agar

1 lution conditions and clonogenic activity in soft agar.

2 ters growth properties and induces growth in soft agar.

3 lls enhanced anchorage-independent growth in soft agar.

4 in the spontaneous formation of colonies in soft agar.

5 ed cells and anchorage-independent growth in soft agar.

6 cacy using two non-tumorigenic cell lines in soft agar.

7 d and several were able to inhibit growth in soft agar.

8 ttenuating their ability to form colonies in soft agar.

9 endent growth of gastric epithelial cells in soft agar.

10 activation, and inhibits the cell growth in soft agar.

11 resensitizes the DDR and restrains growth in soft agar.

12 -dependent tumor cell motility and growth in soft agar.

13 of colony formation, and impaired growth in soft agar.

14 ut had little effect on swimming motility in soft agar.

15 re necessary for TGF-beta-mediated growth in soft agar.

16 , resulting in increased colony formation in soft agar.

17 fewer colonies in both monolayer culture and soft agar.

18 n potential, assessed by colony formation in soft agar.

19 zomib inhibited estrogen-dependent growth in soft agar.

20 etic basement membranes, and their growth in soft agar.

21 UMUC3) were dependent on FGFR1 for growth in soft agar.

22 on and prostate cancer cell colony growth in soft agar.

23 mary epithelial cells caused their growth in soft agar.

24 ing in a viscous medium or on the surface of soft agar.

25 d growth of human glioblastoma T98G cells in soft agar.

26 ayer culture and growth of large colonies in soft agar.

27 one induced little or no colony formation in soft agar.

28 chment conditions analogous to growth in the soft agar.

29 d by a screen for restoration of motility in soft agar.

30 as assessed by measuring colony formation in soft agar.

31 f multiple Wnt-addicted cancer cell lines in soft agar.

32 feration and anchorage-independent growth in soft agar.

33 s tumor cell anchorage-independent growth in soft agar.

34 cancer, BT-20 cells do not form colonies in soft agar.

35 n to inhibit anchorage-independent growth in soft agar.

36 BT-20 cells the ability to form colonies in soft agar.

37 sform primary mouse embryonic fibroblasts in soft agar.

38 roliferation, colony formation and growth in soft agar.

39 erin levels, and reduced colony formation in soft agar.

40 and reduced clonogenicity on plastic and in soft agar.

41 cultures and anchorage-independent growth in soft agar.

42 feration and anchorage-independent growth on soft agar.

43 orage-independent growth of cell colonies on soft agar.

44 red by the ability to form large colonies in soft agar.

45 ells reduces anchorage-independant growth in soft agar.

46 mation in mice, as well as foci formation in soft agar.

47 f v-Rel transformed CEFs to form colonies in soft agar.

48 binant retrovirus suppressed their growth in soft agar.

49 eration, and anchorage-independent growth in soft agar.

50 ble to inhibit HC11-Int3 colony formation in soft agar.

51 59 led to a reduction of colony formation in soft agar.

52 TT assay and anchorage-independent growth in soft agar.

53 tion of the MNKs reduces colony formation in soft agar.

54 melanoma proliferation in both monolayer and soft agar.

55 medium-stimulated epithelial cell growth in soft agar.

56 ted spontaneous mutants able to move through soft agar.

57 s to form xenografts in mice and colonies in soft agar.

58 leus, an overgrowth phenotype, and growth in soft agar.

59 ent on IRS1 activity for colony formation in soft agar.

60 growth and migration and colony formation in soft agar.

61 nes enhances the ability to form colonies in soft agar.

62 of prostate cancer cells to form colonies in soft agar.

63 ration but essential for colony formation in soft agar.

64 cell transformation as assessed by growth in soft agar.

65 atiotemporal dynamics of Escherichia coli in soft agar(12,17,18).

66 nd migration, as well as reduced survival in soft agar (a measure of anoikis).

67 cells and monitored its effects on growth in soft agar, a hallmark of cellular transformation, and al

68 vasiveness and decreased colony formation in soft agar across multiple melanoma cell lines.

69 e ability of these cells to form colonies in soft agar, an in vitro measure of tumorgenicity.

70 ERK and Akt activity and inhibited growth in soft agar and ability of these cells to migrate.

71 morigenic phenotype with increased growth in soft agar and an invasive phenotype in three-dimensional

72 44, and displayed increased clonogenicity in soft agar and broad drug-resistance in vitro and in vivo

73 and FLLL32 also inhibit colony formation in soft agar and cell invasion and exhibit synergy with the

74 nhibition of anchorage-independent growth in soft agar and cell migration in each of four NSCLC lines

75 d cell proliferation and colony formation in soft agar and cell-cycle arrest.

76 c Mullerian epithelial marker genes, grow in soft agar and develop ectopic invasive tumors in recipie

77 s, increased anchorage-independent growth in soft agar and enhanced tumor growth in severe combined i

78 Similar results were seen in soft agar and focus-formation assays, where p110beta was

79 so inhibited anchorage-independent growth in soft agar and growth in an orthotopic xenograft model.

80 on is associated with higher tumor growth in soft agar and in a xenograft model.

81 horage-independent survival of HeLa cells in soft agar and in athymic mice.

82 density, and acquired the ability to grow in soft agar and in Matrigel compared with the parental rel

83 reby, to be essential for melanoma growth in soft agar and in nude mice.

84 roliferation, migration, invasion, growth in soft agar and in vivo tumorigenicity, whereas downregula

85 he ability of neuroblastoma cells to grow in soft agar and induce tumors in immunodeficient mice.

86 ability of neurospheres to form colonies in soft agar and inhibited their capacity to propagate subc

87 H1299 lung cancer cells inhibited growth in soft agar and invasive colony formation in Matrigel and

88 h the MAPK inhibitor U0216 reduced growth in soft agar and invasive phenotype, whereas the combinatio

89 adhesion, cell invasion, colony formation in soft agar and metastasis in a rat model system.

90 y of breast cancer cells to form colonies in soft agar and metastasize to the lungs or liver.

91 olayers, but developed into colonospheres in soft agar and nodules/tumors in nude mice.

92 ormed monolayers as well as colonospheres in soft agar and nodules/tumors in nude mice.

93 mediated CTSD induction, inhibited growth in soft agar and partially restored tamoxifen sensitivity o

94 Long-term-infected TIVE cells (LTC) grew in soft agar and proliferated under reduced-serum condition

95 ir growth rate, enhanced colony formation in soft agar and promoted tumor formation in nude mice.

96 d cells contained HPV-16, formed colonies in soft agar and rapidly produced tumors in immunodeficient

97 ased cell proliferation, colony formation in soft agar and strikingly diminished cell migration and i

98 mutant mtDNA were tested by growth assay in soft agar and subcutaneous implantation of the cells in

99 breast cancer cells in liquid culture and in soft agar and suppresses the tumorigenicity of MCF-7 cel

100 of tumor cell growth and colony formation in soft agar and the extent of such inhibition appeared to

101 cell lines (R(-)3) formed large colonies in soft agar and the transformation of these T antigen-expr

102 utant failed to exhibit swarming motility on soft agar and this phenotype was rescued by a plasmid-bo

103 ability of tumorigenic rat cells to grow in soft agar and to form tumors.

104 ed anchorage-independent colony formation in soft agar and tumor burden in an allograft model.

105 TGM2 suppressed colony formation in soft agar and tumor formation in a xenograft mouse model

106 to impair RasV12-driven colony formation in soft agar and tumor growth in mice.

107 haracteristics and inhibited their growth in soft agar and tumor growth in vivo.

108 epidermoid cancer cells inhibited growth in soft agar and tumorigenesis in nude mice, and suppressed

109 TPA-mediated anchorage-independent growth in soft agar and tumorigenicity in nude mice.

110 5 in HaCaT cells induced colony formation in soft agar and tumorigenicity in nude mice.

111 insult formed significantly more colonies in soft agar and were significantly more invasive when grow

112 clones showed dramatically reduced growth in soft agar and when implanted s.c.

113 ed in the transformation of keratinocytes in soft agar and xenograft establishment, thus also implica

114 eration and reduced both colony formation in soft agar and xenograft tumor growth in immunodeficient

115 rmation activity (focus formation, growth in soft agar) and activation of PI3K and MAPK signaling.

116 rongly stimulated cell growth in culture, in soft agar, and accelerated tumor formation in a ligand i

117 proliferation, abolishes colony formation in soft agar, and decreases NO generation.

118 oliferation, anchorage-independent growth in soft agar, and enhanced metastatic potential.

119 of transformed cells to form clones, grow in soft agar, and form tumors in severe combined immunodefi

120 igher growth rate, produced more colonies in soft agar, and formed larger tumor upon xenograft inject

121 in monolayer culture, suspension culture, or soft agar, and in vivo in tumor xenografts.

122 ncer drug, invasion, and colony formation in soft agar, and in vivo tumor growth in nude mice.

123 A, increased anchorage-independent growth in soft agar, and increased migration.

124 um, enhanced anchorage-independent growth in soft agar, and increased tumorigenicity in nonobese diab

125 feration, enhanced tumor colony formation in soft agar, and increased xenograft tumor growth in nude

126 h cell proliferation and colony formation in soft agar, and induces apoptosis in cancer cells.

127 l proliferation, reduced colony formation in soft agar, and induction of apoptosis.

128 osis in culture, reduced colony formation in soft agar, and inhibited invasion of melanoma cells.

129 ced apoptosis, abolished colony formation in soft agar, and inhibited localized and metastatic tumor

130 pe, acquired anchorage-independent growth in soft agar, and led to enlarged, disorganized, three-dime

131 dine decreased cell proliferation, growth in soft agar, and methylcytosine content of malignant chola

132 V-induced proliferation, colony formation in soft agar, and NO generation of KSHV-transformed cells,

133 cycle progression, small colony formation in soft agar, and no tumor formation in nude rats.

134 er, HBx stimulated cell migration, growth in soft agar, and spheroid formation.

135 growth rate in culture, colony formation in soft agar, and tumor progression in nude mice.

136 oliferation, anchorage-independent growth in soft agar, and tumorigenesis in severe combined immunode

137 m foci in tissue culture plates, colonies in soft agar, and tumors in nude mice.

138 itro cell proliferation, colony formation in soft agar, and xenograft growth in athymic mice.

139 of cell proliferation, migration, growth in soft agar, apoptosis, senescence, and gene expression re

140 r growth of human pancreatic cancer cells in soft agar as well as in athymic nude mice.

141 Results obtained using a soft agar assay and shRNA Nrf2-transfected cells show th

142 w the anticancer activity of SC66 by using a soft agar assay as well as a mouse xenograft tumor model

143 Transformation in a single layer soft agar assay could be documented as early as 2 to 3 d

144 ndependent cell growth ability was tested by soft agar assay following FA exposure.

145 Because the soft agar assay is unsuitable for high throughput screen

146 The soft agar assay was used as a measure of anchorage indep

147 In a soft agar assay, treatment of HC11-Int3 cells with P50-s

148 anchorage-independent growth as revealed by soft agar assay.

149 Cell transformation was assessed by soft agar assay.

150 nditions and is strongly correlated with the soft-agar assay.

151 ntified and tumorigenesis was assessed using soft agar assays and xenograft analysis of severe combin

152 Soft agar assays revealed that anchorage-independent gro

153 A has transforming activities when tested in soft agar assays, and CoAA is homologous to oncoproteins

154 as evidenced by enhanced colony formation in soft agar assays.

155 s, and blocked contact-independent growth in soft agar assays.

156 is BRCA1 dependent shown by 3D-matrigel and soft agar assays.

157 K knockdown in a xenotransplant model and in soft agar assays.

158 Lin28 was determined by colony formation and soft agar assays.

159 sed the colony formation of human T cells in soft-agar assays.

160 invasive properties, and formed colonies in soft-agar assays.

161 d cell proliferation and colony formation in soft-agar assays.

162 anchorage-independent growth by conducting a soft agar-based short hairpin RNA (shRNA) screen within

163 hibits Src-Y527F-induced colony formation in soft agar, but not Ras-G12V-induced colony formation.

164 y formation, anchorage-independent growth in soft agar, cell migration, and epithelial-mesenchymal tr

165 ates of cell proliferation, clonogenicity in soft agar, changes in the actin cytoskeleton, and induct

166 additional novel DNA methylation targets in soft-agar clones derived from CSC-exposed HBEC; a CSC ge

167 The soft agar clonogenic assay showed that T80/KLF8 cells fo

168 1 in cultured SCLC resulted in inhibition of soft agar clonogenic capacity and induction of apoptosis

169 d tumor cells showed significantly increased soft-agar clonogenic ability and tumor sphere formation.

170 by CSC coincided with a dramatic increase in soft-agar clonogenicity.

171 Soft agar colonies of CLP-expressing cells had rough bou

172 n, glycolytic flux to lactate, and growth as soft agar colonies or tumors in athymic mice.

173 hat have undergone an EMT form mammospheres, soft agar colonies, and tumors more efficiently.

174 horylated at Ser79/81 (S79/81A) formed fewer soft agar colonies.

175 nhibited but were unable to efficiently form soft-agar colonies or tumor xenografts, suggesting that

176 s apoptosis and suppresses proliferation and soft agar colonization.

177 cts of Bcr-Abl in a solid tumor model and in soft agar colony assays.

178 rming Matrigel invasion, cell proliferation, soft agar colony formation and scratch closure assays.

179 Soft agar colony formation assays and xenograft studies

180 ion in EBER-expressing cells was examined in soft agar colony formation assays.

181 cells and mouse epidermal JB6 cells promoted soft agar colony formation by downregulating Pdcd4 prote

182 or chemical inhibition of Gln uptake blocks soft agar colony formation by Hace1(-/-) MEFs.

183 d with reduced in vitro proliferation rates, soft agar colony formation efficiency, and migration rat

184 lls by TSC2 siRNA, and decreased Myc-induced soft agar colony formation following retroviral transduc

185 t FGF19 could promote cell proliferation and soft agar colony formation in HNSCC cells with low FGF19

186 growth factor-independent proliferation and soft agar colony formation in MCF10A cells, and hLsm1 in

187 protein function decreased proliferation and soft agar colony formation of ESFT cells.

188 of profibrotic targets, cell migration, and soft agar colony formation stimulated by TGF-beta requir

189 ransition) signaling, transwell invasion and soft agar colony formation, and in vivo promoted lung me

190 ets of miR-7, reduced cell proliferation and soft agar colony formation, and increased apoptosis.

191 associated with altered cellular phenotypes, soft agar colony formation, and tumorigenesis in nude mi

192 2-yl)-2,5-diphenyltetrazolium bromide assay, soft agar colony formation, as well as tumor growth in a

193 ificantly suppresses cell growth in culture, soft agar colony formation, cell invasion and growth of

194 ion of wild-type full-length TMEFF2 inhibits soft agar colony formation, cellular invasion, and migra

195 sive SK-N-SH neuroblastoma cells resulted in soft agar colony formation, which was inhibited by a GRP

196 ells led to decreased transwell invasion and soft agar colony formation, without affecting proliferat

197 ibited their growth, motility, invasion, and soft agar colony formation.

198 ation, or cell transformation as measured by soft agar colony formation.

199 shRNAs leads to increased proliferation and soft agar colony formation.

200 C downregulation increased cell invasion and soft agar colony formation; this was dependent on NF-kap

201 co-expression of PEA-15 resulted in enhanced soft agar colony growth and increased tumor growth in vi

202 Soft agar colony growth assays were applied to examine i

203 stable suppression of RalB greatly enhanced soft agar colony size and formation frequency.

204 enhancement of cell proliferation, increased soft agar colony size, and elevated ERK1/2 phosphorylati

205 lls and completely blocks their invasive and soft agar colony-forming abilities, but it spares nontra

206 A soft-agar colony assay showed that PLK1 silencing impair

207 SHP2 activity attenuates cell proliferation, soft-agar colony formation and orthotopic GBM growth in

208 but not CRAF WT, transformed NIH3T3 cells in soft-agar colony formation assays, increased kinase acti

209 investigated using mammosphere formation and soft-agar colony formation assays.

210 c cooperate in suppressing proliferation and soft-agar colony formation of neoplastic epithelial ovar

211 in vitro proliferation, migration, invasion, soft-agar colony formation, and survival in the presence

212 ckdown of CDH10 promoted cell proliferation, soft-agar colony formation, cell migration and cell inva

213 imatinib-induced apoptosis and inhibition of soft-agar colony formation.

214 resulted in impaired in vitro migration and soft-agar colony formation.

215 NT-3 promoted motility, migration, invasion, soft-agar colony growth and cytoskeleton restructuring i

216 re also increased cell growth as assessed by soft-agar colony survival and cell growth assays, and pr

217 icantly improved ability to form colonies in soft agar compared with control.

218 P cells had little colony-forming ability in soft agar compared with TonB210/GFP cells.

219 invasion, motility, and colony formation in soft agar compared with vector control-transfected cells

220 Assays on soft-agar confirmed that NsrR is a negative regulator of

221 unction inhibits PC3 growth in monolayer and soft agar cultures.

222 ced SmgGDS expression form fewer colonies in soft agar, do not proliferate in culture due to an arres

223 These cells when trypsinized and regrown in soft agar, formed colonospheres/organoids that developed

224 melanocytes grew anchorage-independently in soft agar, formed pigmented lesions reminiscent of in si

225 neuploidy, and amplified colony formation in soft agar, further supporting the role of CHFR as a tumo

226 nement of a worm between a glass plate and a soft agar gel is controlled while recording the worm's m

227 x2 was necessary for its ability to increase soft agar growth and in vivo metastasis in an immunocomp

228 n of ZNF322A promoted cell proliferation and soft agar growth by prolonging cell cycle in S phase in

229 from CAN-genes, and experimentally verifying soft agar growth enhancement in response to depletion of

230 r in combination and observed the effects on soft agar growth of HC11 cells overexpressing Int3.

231 f the ITSN1 target, PI3K-C2beta, rescues the soft agar growth of ITSN1-silenced cells demonstrating t

232 owth inhibitory effects of TGF-beta, and the soft agar growth of these cells was increased upon TGF-b

233 Synergistic inhibition of soft agar growth was also observed.

234 d signaling pathways regulate proliferation, soft agar growth, and invasion of human lung adenocarcin

235 essed HBECs toward malignancy as measured by soft agar growth, including EGF-independent growth, but

236 ted resistance to redox stress and increased soft agar growth, while downregulation of SQSTM1 decreas

237 only 5 of 362 random shRNAs (1.4%) enhanced soft agar growth.

238 hibition in SUM44 cells dramatically reduced soft agar growth.

239 d bone matrix-related filaments and enhanced soft agar growth.

240 ble knockdown of SLFN2 form more colonies in soft agar, implicating this protein in the regulation of

241 Also IGF1 enhanced colony formation in soft agar in an alpha6beta4-dependent manner.

242 in human melanoma cells inhibited growth on soft agar in vitro and tumor formation in vivo, suggesti

243 ) cells enhanced proliferation and growth in soft agar in vitro but was insufficient to drive tumorig

244 reased the ability of these cells to grow in soft agar in vitro.

245 e Escherichia coli populations in semisolid (soft) agar in the concentration range C = 0.15-0.5% (w/v

246 ed increased anchorage-independent growth in soft agar, increased S-phase cell cycle distribution, in

247 creased Wnt activity and colony formation in soft agar induced by Apc siRNA treatment, whereas they d

248 f tumor cell anchorage-independent growth in soft agar, induction of the p130Cas cleavage, and anoiki

249 al for malignant transformation according to soft agar, invasion, and tumorigenicity assays, after th

250 he ability of breast cancer cells to grow in soft agar is enhanced following GREB1 transfection.

251 Colony formation in soft agar is the gold-standard assay for cellular transf

252 mutants for those that could migrate through soft agar medium lacking added magnesium.

253 catechin-3-gallate (EGCG) inhibits growth in soft agar of breast cancer cells with Her-2/neu overexpr

254 phosphorylated ERK, and slows the growth in soft agar of HCT116 cells.

255 d cell proliferation and colony formation in soft agar of KSHV-transformed cells by attenuating mTORC

256 and obese human donors stimulated growth in soft agar of non-tumorigenic epithelial cells.

257 es individually promoted colony formation in soft agar or collaborated with each other functionally.

258 d RBM3 is downregulated in cells cultured in soft agar or exposed to stress.

259 to transform normal cells enabling growth in soft agar or in immunodeficient mice.

260 the ability of C6 cells to form colonies in soft agar or spheres when grown in suspension.

261 pressing populations do not form colonies in soft agar or tumors in mice.

262 strain G27 resulted in decreased motility on soft agar plates, a defect that was complemented by a wi

263 invasion and anchorage-independent growth on soft agar plates.

264 rly flagellated counterparts in spreading on soft-agar plates and through medium-filled channels desp

265 gand-independent proliferation and growth in soft agar relative to cells expressing wt PR-B or phosph

266 Similarly, cell growth in soft agar required the PR DBD but was sensitive to disru

267 ack EP2 expression prevented their growth in soft agar, restored their cytostatic response to TGF-bet

268 ever, including impaired colony formation in soft agar, spheroid formation, and xenograft growth.

269 genesis as measured by growth of colonies in soft agar, spheroids in extracellular matrix and xenogra

270 orage-independent cell transformation assay (soft agar), stable expression of RSK2 in JB6 cells signi

271 iferation, promoted formation of colonies in soft agar, stimulated tumor cell invasion, and induced l

272 opment of compact multicellular spheroids in soft agar suggesting the ability to induce anchorage-ind

273 d prostate cells enabled colony formation in soft agar, suggesting that, in the proper cellular conte

274 -ras allele consistently increased growth in soft agar, suggesting tumor-suppressive properties of th

275 motile and non-motile bacterial species on a soft agar surface.

276 , AgmU-mCherry clusters were not observed on soft agar surfaces or when cells were in large groups, c

277 g GRP78 and Cripto grow much more rapidly in soft agar than do cells expressing either protein indivi

278 significantly fewer and smaller colonies in soft agar than their 2D-irradiated counterparts (gamma P

279 ant transformation, as measured by growth in soft agar, the gold-standard in vitro transformation ass

280 93a controls anchorage-independent growth in soft agar through K-Ras, whereas it affects invasive gro

281 In the soft agar transformation and Transwell metastasis assays

282 e, as shown by increased colony formation in soft agar, tumor formation in SCID (severe combined immu

283 invasion and anchorage-independent growth in soft agar, two fundamental biological events associated

284 ersely, silencing RBM3 or culturing cells in soft agar (under conditions that enrich for stem cell-li

285 PTEN into PEL inhibited colony formation in soft agar, verifying the functional dependence of PEL on

286 cant 3-fold increase in clonogenic growth in soft agar was also noted.

287 y, swarming from colonies grown on MacConkey soft agar was delayed in the mutant in comparison to the

288 Growth of transformed cells in soft agar was enhanced by alpha-4 and suppressed by alph

289 Colony formation by RCC 786-O in soft agar was markedly inhibited by DPI.

290 colonies of the NSCLC cell line, H1,299, in soft agar was strongly inhibited by the Abl kinase inhib

291 li in liquid and embedded in glucose-limited soft agar, we evaluate the fit of this model to experime

292 -7 cells for anchorage independent growth in soft agar were dependent on GIT1.

293 prevents HeLa cells from forming colonies in soft agar, when paxillin is knocked down together with C

294 e cells), and these cells formed colonies in soft agar, whereas BCR-ABL+ NIH 3T3 cells lacking IL-3 r

295 s promotes their ability to form colonies in soft agar, whereas ectopically expressing paxillin in th

296 ll lines to proliferate and form colonies in soft agar, whereas EWSAT1 inhibition had no effect on ot

297 ion through collagen and decreased growth in soft agar, whereas the second was enriched in cells with

298 nduced colony formation of JB6 Cl41 cells in soft agar, which was associated with inhibition of histo

299 o stimulated cancer cell colony formation in soft agar, which was reduced by a chemical inhibitor of

300 igration, invasion, and colony formation, in soft agar with CD66(high) cells.